Goal-Directed Therapy in Pregnant Women at High Risk of Developing Preeclampsia
|The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details.|
|ClinicalTrials.gov Identifier: NCT01351428|
Recruitment Status : Completed
First Posted : May 10, 2011
Last Update Posted : November 12, 2012
Preeclampsia is associated with significant maternal and fetal morbidity and mortality. Early identification and subsequent management of patients at risk of developing preeclampsia presents an ongoing challenge in prenatal care. Some at risk pregnancies may be identified from:
- serum screening abnormalities in the first or second trimester
- placental shape and texture at the 18-20 anatomical ultrasound
- uterine artery blood flow.
Early identification and effective treatment of patients would permit the safe completion of the pregnancy for the mother and infant. Recent advances in non-invasive cardiovascular monitoring have enabled the study of maternal hemodynamics in normal and at-risk pregnancies. This study hopes to identify the earliest significant changes in maternal hemodynamics which may allow targeted therapeutic interventions in patients at high risk of developing preeclampsia.
The hypothesis of this study is that systemic vascular resistance rises during the pre-clinical phase of preeclampsia and this can be captured using non invasive bioreactance technology. Treatment of the abnormally high vascular tone may decrease the severity and postpone the onset of clinical disease.
|Condition or disease||Intervention/treatment||Phase|
|Pre-Eclampsia Pregnancy Hypertension||Drug: Nifedipine||Not Applicable|
Invasive hemodynamic techniques have long identified significant increases in heart rate (HR), blood volume, left ventricular end-diastolic volume (LVEDV), stroke volume (SV) and cardiac output (CO) during the first and second trimesters of pregnancy. In normal pregnancy, CO increases from as early as 5 weeks gestation, with a 30-40% increase by the end of the first trimester of pregnancy. Cardiac output continues to rise throughout the second trimester until it reaches a level approximately 50% greater than that of non-pregnant women. Cardiac output slightly decreases during the third trimester. Despite these changes, maternal blood pressure (BP) still falls due to a large reduction in systemic vascular resistance (SVR) from systemic vasodilatation and the formation of a low-resistance utero-placental circulation. Systemic vascular resistance falls during early gestation, reaching its nadir (35% decline) at 20 weeks gestation, and rises during late pregnancy.
Transthoracic bioreactance is a newer technique of non-invasive continuous cardiac output monitoring. It is based on an analysis of relative phase shifts of oscillating currents that occur when this current traverses the thoracic cavity, as opposed to the traditional bioimpedance-based system, which rely only on measured changes in signal amplitude. Unlike bioimpedance, bioreactance-based non-invasive CO measurement does not use the static impedance and does not depend on the distance between the electrodes for the calculations of SV and CO, which significantly reduces the uncertainty in the result. Moreover, its readings were shown to correlate well with results derived from pulmonary artery catheter derived measurement of cardiac output. In addition, it has also been shown that the non-invasive cardiac output measurement (NICOM®) system has acceptable accuracy, precision and responsiveness for CO monitoring in patients experiencing a wide range of circulatory situations and has recently been used in the obstetric population.
The purpose of this study is to use non-invasive cardiac output monitoring to capture the earliest inappropriate rise in SVR during the pre clinical phase of disease, in patients at high risk of developing preeclampsia, as predicted by the placenta profile. In case an increase in SVR is identified, the purpose of this study is to implement a goal-directed therapy in an attempt to decrease the severity, and postpone the onset of clinical disease.
The hypothesis of this study is that the increases in SVR detected during the pre-clinical phase of preeclampsia can be treated with a goal directed therapy without fetal compromise and that this intervention may improve maternal and fetal/neonatal outcome.
|Study Type :||Interventional (Clinical Trial)|
|Actual Enrollment :||20 participants|
|Intervention Model:||Single Group Assignment|
|Masking:||None (Open Label)|
|Official Title:||Non-invasive Hemodynamic Monitoring and Goal-Directed Therapy in Pregnant Women at High Risk of Developing Preeclampsia|
|Study Start Date :||December 2010|
|Actual Primary Completion Date :||November 2012|
|Actual Study Completion Date :||November 2012|
Experimental: NICOM group
Vasodilator therapy begins when SVR increases by 20% or greater than baseline. Therapy is titrated according to hemodynamic profile and clinical signs and symptoms.
30-60 mg, twice daily
Other Name: Adalat XL
- Systemic vascular resistance [ Time Frame: 20-22, 24-26, 28, 30-32 and 36 weeks gestational age ]Systemic vascular resistance is measured at the above time points, and more frequently at the discretion of the attending obstetrician.
- Maximum change in maternal blood pressure [ Time Frame: 20-22, 24-26, 28, 30-32 and 36 weeks gestational age ]Blood pressure is taken on the NICOM at the above time points, and more frequently at obstetric appointments in between.
- Gestational age at delivery [ Time Frame: 25-41 weeks gestational age ]
- Fetal weight at delivery [ Time Frame: 25-41 weeks gestational age ]
- Gestational age at time of first hospitalization [ Time Frame: 25-41 weeks gestational age ]
- Gestational age at peak maternal blood pressure [ Time Frame: 20-41 weeks ]
- Gestational age at which steroids are administered [ Time Frame: 25-41 weeks gestational age ]
- Serum s-Flt and PlGF levels [ Time Frame: 12-41 weeks gestational age ]
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT01351428
|Mount Sinai Hospital|
|Toronto, Ontario, Canada, M5G1X5|
|Principal Investigator:||Jose CA Carvalho, MD||Mount Sinai Hospital, New York|